AI Article Synopsis
- - The study identifies the TRIM25 gene's role in COVID-19, revealing that lower expression levels of this gene are linked to more severe disease outcomes compared to milder cases and healthy individuals.
- - The research involved analyzing blood samples from 330 COVID-19 patients and 160 healthy individuals, using quantitative Real-time PCR to assess TRIM25 expression and its correlation with disease severity.
- - Results indicate that increased TRIM25 expression can reduce SARS-CoV-2 virus replication and promote immune response by inducing beta-interferon, highlighting its potential as a therapeutic target for COVID-19 treatment.
Article Abstract
Background: There are numerous human genes associated with viral infections, and their identification in specific populations can provide suitable therapeutic targets for modulating the host immune system response and better understanding the viral pathogenic mechanisms. Many antiviral signaling pathways, including Type I interferon and NF-κB, are regulated by TRIM proteins. Therefore, the identification of TRIM proteins involved in COVID-19 infection can play a significant role in understanding the innate immune response to this virus.
Methods: In this study, the expression of TRIM25 gene was evaluated in a blood sample of 330 patients admitted to the hospital (142 patients with severe disease and 188 patients with mild disease) as well as in 160 healthy individuals. The relationship between its expression and the severity of COVID-19 disease was assessed and compared among the study groups by quantitative Real-time PCR technique. The statistical analysis of the results demonstrated a significant reduction in the expression of TRIM25 in the group of patients with severe infection compared to those with mild infection. Furthermore, the impact of increased expression of TRIM25 gene in HEK-293 T cell culture was investigated on the replication of attenuated SARS-CoV-2 virus.
Results: The results of Real-time PCR, Western blot for the viral nucleocapsid gene of virus, and CCID test indicated a decrease in virus replication in these cells. The findings of this research indicated that the reduced expression of the TRIM25 gene was associated with increased disease severity of COVID-19 in individuals. Additionally, the results suggested the overexpression of TRIM25 gene can impress the replication of attenuated SARS-CoV-2 and the induction of beta-interferon.
Conclusion: TRIM25 plays a critical role in controlling viral replication through its direct interaction with the virus and its involvement in inducing interferon during the early stages of infection. This makes TRIM25 a promising target for potential therapeutic interventions.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jiph.2024.102489 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Targeting UBE2T suppresses breast cancer stemness through CBX6-mediated transcriptional repression of SOX2 and NANOG.
Cancer Lett
December 2024
Department of General Surgery, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China; Cuiying Biomedical Research Center, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China; Gansu Province High-Altitude High-Incidence Cancer Biobank, The Second Hospital of Lanzhou University, Lanzhou, Gansu, China. Electronic address:
Breast cancer stem cells (BCSCs) are the main cause of breast cancer recurrence and metastasis. While the ubiquitin-proteasome system contributes to the regulation of BCSC stemness, the underlying mechanisms remain unclear. Here, we identified ubiquitin-conjugating enzyme E2T (UBE2T) as a pivotal ubiquitin enzyme regulating BCSC stemness through systemic screening assays, including single-cell RNA sequencing (scRNA-seq) and stemness-index analysis.
View Article and Find Full Text PDFNF-kappa B signaling pathway is associated with metformin resistance in type 2 diabetes patients.
J Diabetes Metab Disord
December 2024
Proteomics Research Center, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Introduction: Metformin is an essential medicine that is most widely prescribed frontline for the treatment of Type 2 diabetes (T2D). Metformin upgraded glycemic control in T2D patients without hypoglycemic effects in patients. This assessment aims to understand molecular mechanism mechanisms in non-responder patients to metformin.
View Article and Find Full Text PDFBMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization.
Mol Med
November 2024
Department of Clinial Laboratory, Capital Medical University Affiliated Beijing Jishuitan Hospital, Xinjiekou No. 31 East Street, Xicheng District, Beijing, 100035, People's Republic of China.
Osteoporosis is characterized by reduced bone mass due to imbalanced bone metabolism. Exosomes derived from bone mesenchymal stem cells (BMSCs) have been shown to play roles in various diseases. This study aimed to clarify the regulatory function and molecular mechanism of BMSCs-derived exosomes in osteogenic differentiation and their potential therapeutic effects on osteoporosis.
View Article and Find Full Text PDFThe microprotein HDSP promotes gastric cancer progression through activating the MECOM-SPINK1-EGFR signaling axis.
Nat Commun
September 2024
Suzhou Cancer Center Core Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, 215001, China.
Article Synopsis
- The study identifies a small protein derived from long non-coding RNAs, called HDSP, that is linked to gastric cancer.
- HDSP promotes cancer by preventing the degradation of MECOM, which then increases the transcription of SPINK1, a gene that activates cancer-related signaling pathways.
- Targeting HDSP either by knocking it down or using it as a neoantigen enhances anti-tumor immunity and suggests it could be a new therapeutic target for treating gastric cancer.
Ubiquitination of ATAD3A by TRIM25 exacerbates cerebral ischemia-reperfusion injury via regulating PINK1/Parkin signaling pathway-mediated mitophagy.
Free Radic Biol Med
November 2024
Department of Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, Liaoning Province, 116044, PR China. Electronic address:
Article Synopsis
- Cerebral ischemia-reperfusion injury (CI/RI) leads to neuronal damage, with mitophagy's role in this process still debated.
- The study hypothesized that TRIM25 enhances mitophagy through the ubiquitination of ATAD3A, aggravating CI/RI.
- Experiments demonstrated that TRIM25 reduces ATAD3A, promoting mitophagy via the PINK1/Parkin pathway, and highlighting a complex interaction between these proteins during ischemic injury.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!